Evidence map›Paper›PMID 21435439›Full record

ArticleThe American journal of pathology2011

Essential role of MeCP2 in the regulation of myofibroblast differentiation during pulmonary fibrosis.

Biao Hu, Mehrnaz Gharaee-Kermani, Zhe Wu, Sem H Phan

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.4field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 98 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. DNA methylation modification in Idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024
    Review
  5. Article
  6. Article
  7. Fibrosis-the tale of H3K27 histone methyltransferases and demethylases.Frontiers in cell and developmental biology · 2023
    Review
  8. DNA methylation in pulmonary fibrosis and lung cancer.Expert review of respiratory medicine · 2022
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. More than a Genetic Code: Epigenetics of Lung Fibrosis.Molecular diagnosis & therapy · 2020
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Biao HuDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109-2200, USA.
Mehrnaz Gharaee-Kermani
Zhe Wu
Sem H Phan
University of Michigan · US

Funding

PUBLIC HEALTH DEMONSTRATIONP60DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 1985 to 2012
$26.5M
Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID P OLSON · 2013 to 2026
$24.3M
MONONUCLEAR LEUKOCYTE ADHESION AND RECRUITMENT IN CHRONIC INFLAMMATORY DISEASEP01HL031963 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JOHNSON, KENT JOHN · 1985 to 2009
$14.1M
Translational control of the fibroblast phenotype in IPFP01HL091775 · NHLBI · UNIVERSITY OF MINNESOTA · PI INGBAR, DAVID H · 2009 to 2013
$8.3M
MYOFIBROBLASTS IN PULMONARY FIBROSISR01HL052285 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 1994 to 2017
$5.4M
Mechanisms of Pulmonary FibrosisR37HL028737 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 2001 to 2010
$3.0M
Novel telomerase expressing lung fibroblast phenotypeR01HL077297 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 2004 to 2012
$3.0M
MECHANISMS OF PULMONARY FIBROSISR01HL028737 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 1986 to 2000
$227k
NHLBI NIH HHS HL28737NHLBI NIH HHS HL31963NHLBI NIH HHS HL52285NHLBI NIH HHS HL77297NHLBI NIH HHS HL91775NHLBI NIH HHS P01 HL031963NHLBI NIH HHS P01 HL091775NHLBI NIH HHS R01 HL028737NHLBI NIH HHS R01 HL052285NHLBI NIH HHS R01 HL077297NHLBI NIH HHS R37 HL028737NIDDK NIH HHS DK020572NIDDK NIH HHS P30 DK020572NIDDK NIH HHS P60 DK020572
6 · The paper itself

Abstract

DNA methylation is a key mechanism for repression of gene expression, including that of α-smooth muscle actin (α-SMA) gene expression in fibroblasts. However, the trans-acting factors that interact with the methylated α-SMA gene to regulate its expression have not been identified. Using gel shift and chromatin immunoprecipitation (ChIP) assays, methyl CpG binding protein 2 (MeCP2) was shown to bind to the α-SMA gene. Suppression of MeCP2 gene expression by siRNA or its deficiency in lung fibroblasts isolated from MeCP2 knockout mice caused significant reduction of α-SMA gene expression. In contrast, transient transfection of MeCP2 expression plasmid into fibroblasts enhanced α-SMA gene expression. Moreover, in vivo studies revealed that compared to their wild type littermates, MeCP2-deficient mice exhibited significantly decreased alveolar wall thickness, inflammatory cell infiltration, interstitial collagen deposition, and myofibroblast differentiation in response to endotracheal injection of bleomycin. Thus, MeCP2 is essential for myofibroblast differentiation and pulmonary fibrosis.

Indexed as

AnimalsBleomycinCell DifferentiationChromatin ImmunoprecipitationFemaleGenes, ReporterHumansLungMethyl-CpG-Binding Protein 2MiceMyofibroblastsPulmonary FibrosisRatsRats, Inbred F344Reverse Transcriptase Polymerase Chain ReactionRNA, MessengerBleomycinMethyl-CpG-Binding Protein 2RNA, Messenger

Identifiers

PMID21435439
PMCPMC3078459
OpenAlexW2026639078

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.